Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine the role of atrial stretch and vasopressin in opiate-induced atrial natriuretic peptide (ANP) release, we studied the effects of a mu receptor agonist fentanyl on plasma immunoreactive ANP (IR-ANP) and hemodynamics (mean arterial pressure, heart rate and right atrial pressure) in the conscious, chronically cannulated Wistar, Long-Evans (LE) and vasopressin-deficient Brattleboro (DI) rats. Infusion of fentanyl (3 and 10 micrograms/kg i.v.) produced an immediate decrease in heart rate in conscious Wistar rats, whereas mean arterial pressure did not change significantly. Heart rate returned to control levels within 2 min of the injection, except after the largest dose of fentanyl when heart rate remained decreased for 5 min. Administration of 10 micrograms/kg of fentanyl caused a marked increase in right atrial pressure (3.9 +/- 0.3 mm Hg, n = 9, P less than .001) associated with 3.5-fold increase in the plasma IR-ANP concentration (168 +/- 17 pg/ml vs. 567 +/- 116 pg/ml, n = 9, P less than .01). In contrast, right atrial pressure decreased by 0.8 +/- 0.3 mm Hg (P less than .05) in response to infusion of 3 micrograms/kg of fentanyl with a slight increase (34%) in plasma IR-ANP. One microgram per kilogram i.v. of fentanyl had no effect on hemodynamic variables and plasma IR-ANP levels. Infusion of V1 antagonist (5 micrograms/kg/min for 25 min) did not affect basal or fentanyl-stimulated changes in hemodynamics or plasma IR-ANP concentration in Wistar rats. Infusion of fentanyl (3 and 10 micrograms/kg) in the LE and DI rats produced similar short-lasting heart rate reductions as seen in Wistar rats. Furthermore, injection of 10 micrograms/kg of fentanyl decreased blood pressure and increased plasma IR-ANP and right atrial pressure in both strains. The analysis of changes in plasma IR-ANP and right atrial pressure in response to fentanyl showed that for a given increase in right atrial pressure, a smaller amount of IR-ANP was released in the DI than in the LE rats. These results demonstrate that at higher fentanyl doses, the increased ANP release is mediated primarily by elevation of right atrial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanism of opioid-induced atrial natriuretic peptide release in conscious rats. 214 37

A diuretic effect of the pentapeptide BW942C [Tyr-D-Met(O)-Gly-pNO2-Phe-Pro-NH2 HCl] was demonstrated in humans and rats; it was characterized pharmacologically using whole animal, isolated tissue and in vitro binding studies. A single 2-mg dose of BW942C increased urine output 5-fold over control values in humans. In Long-Evans rats, BW942C produced a biphasic dose-response curve for urine output with lower doses increasing and higher doses suppressing output. Low doses of naltrexone antagonized the antidiuresis, and high doses antagonized the diuresis produced by BW942C. BW942C was less efficacious in producing diuresis than the full kappa agonists bremazocine and U50,488H (trans-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]- benzeneacetamide methanesulfonate, hydrate). Furthermore, BW942C antagonized the diuretic effects of bremazocine and U50,488H. Rats tolerant to U50,488H-induced diuresis were cross-tolerant to BW942C. In Brattleboro rats, which are unable to synthesize vasopressin, BW942C failed to produce a diuretic effect, demonstrating the necessity of vasopressin for its diuretic response. In the kappa-selective rabbit vas deferens bioassay, BW942C was less efficacious than a full agonist, it was antagonized by naloxone and BW942C in nondepressant doses antagonized a full agonist. In binding studies, BW942C had the highest affinity for mu and delta opioid receptors and an intermediate affinity for kappa opioid receptors. The data suggest that BW942C has the property of a partial kappa opioid agonist in addition to being a mu agonist.
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PMID:Kappa opioid partial agonist activity of the enkephalin-like pentapeptide BW942C based on urination and in vitro studies in humans and animals. 215 1

Regional hemodynamic responses to bolus doses (4 and 40 pmol) and 60-min infusions (12 and 120 pmol/h) of endothelin-2 (ET-2) and sarafotoxin-S6b (S6b) were measured in conscious Long-Evans and Brattleboro rats chronically instrumented with pulsed Doppler flow probes. In both strains of rat the two bolus doses of ET-2 and S6b peptides caused an initial fall in mean blood pressure (MBP). At the higher dose S6b caused a greater fall in MBP than ET-2. In Long-Evans rats the fall in MBP after S6b was associated with renal, mesenteric, and hindquarters vasodilatations; in Brattleboro rats there was no renal or mesenteric vasodilatation with S6b. The high dose of ET-2 caused early mesenteric vasoconstriction in both strains. After the initial fall in MBP there were dose-dependent increases in MBP together with renal and mesenteric vasoconstrictions. These effects were generally greater after S6b than after ET-2 and no less marked in Brattleboro than in Long-Evans rats, indicating that release of endogenous vasopressin was not an indispensable component of the response. Infusions of the higher dose of ET-2 or S6b caused increases in MBP only, associated with renal, mesenteric, and hindquarters vasoconstrictions. The results indicate that S6b is a more potent stimulus than ET-2 of vasodilator mechanisms in vivo; despite this, S6b also exerts more marked vasoconstrictor effects than ET-2.
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PMID:Regional hemodynamic effects of endothelin-2 and sarafotoxin-S6b in conscious rats. 218 84

The effects on coeliac and superior mesenteric blood flows of intravenous bolus doses of arginine-8-vasopressin (0.7 and 7.0 pmol) porcine neuromedin U-25 (0.01 and 1.0 nmol), rat alpha-calcitonin gene-related peptide (0.05 and 0.5 nmol), bombesin (0.06 and 0.6 nmol), and rat corticotropin-releasing factor (1.0 and 5.0 nmol) were investigated in conscious, Long-Evans rats chronically instrumented with pulsed Doppler flow probes. The peptides investigated were chosen on the basis of the range (vasoconstrictor-vasodilator) of their effects on superior mesenteric blood flow. With the exception of rat corticotropin-releasing factor (which increased coeliac and superior mesenteric flows) all peptides caused directionally opposite changes in coeliac and superior mesenteric blood flows. The results are consistent with the proposition that endogenous neuropeptides could influence blood flows to different abdominal viscera selectively.
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PMID:Differential effects of neuropeptides on coeliac and superior mesenteric blood flows in conscious rats. 221 3

Tritiated arginine8-vasopressin [( 3H]AVP) was used to identify specific binding sites for this neuropeptide in the CNS of the golden hamster. [3H]AVP binding sites were concentrated in the dorsal, ventral and lateral septum, bed nucleus of the stria terminalis (BNST), central amygdala, hippocampus, dorsal thalamic nuclei, anterior cingulate gyrus and endopiriform nucleus. Septal-BNST [3H]AVP binding sites were further characterized using membrane preparations. Saturation analysis in septal-BNST membranes resulted in a Bmax of 12.4 +/- 0.82 fmol/mg protein and a Kd of 2.5 +/- 0.36 nM. Pharmacological studies indicate that the binding site in the septum-BNST membranes shows selectivity similar to a V1-type vasopressin receptor. Binding characteristics were similar to those obtained from crude septal membranes prepared from adult Long-Evans rat.
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PMID:[3H]arginine-vasopressin binding sites in the CNS of the golden hamster. 228 Aug 96

An extracorporeal circulation technique was developed for use in rats to provide equilibrated blood samples for multiple hormone assays. The inclusion of the extracorporeal circulation did not significantly alter arterial blood pressure, cardiac output, heart rate or central venous pressure in either Brattleboro rats with hereditary diabetes insipidus (BDI) or normal rats of the parent Long Evans (LE) strain. Plasma adrenaline and noradrenaline levels did not alter in either BDI or LE rats following inclusion of the extracorporeal circulation but the vasopressin concentration rose significantly in the LE rats. The impaired recovery of the mean arterial blood pressure following haemorrhage in the BDI rats compared with normal LE animals was not further influenced by the inclusion of the extracorporeal circulation. Plasma vasopressin and adrenaline (but not nor-adrenaline) levels were significantly raised during, and after, haemorrhage in the LE rats while in the BDI rats only plasma adrenaline levels were significantly increased. These results show that the insertion of an extracorporeal circulation into an anaesthetized BDI or LE rat does not adversely affect the cardiovascular system despite the increase in baseline plasma vasopressin concentration in normal rats, and its subsequent removal provides an additional equilibrated blood sample for multiple hormone assay within the same animal. The increased release of both adrenaline and vasopressin (but not noradrenaline) after haemorrhage in the same animal is detected using this technique, and the importance of vasopressin to the normal recovery process confirmed.
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PMID:Cardiovascular and hormonal changes following haemorrhage in the anaesthetized Brattleboro rat with an extracorporeal circulation. 229

In conscious unrestrained Long-Evans rats, chronically instrumented with miniaturized pulsed Doppler flow probes, intravenous administration of porcine neuromedin U-8 by bolus (0.1 and 1.0 nmol) or infusion (1 and 10 nmol/h) exerted potent constrictor effects on the superior mesenteric vascular bed. With the choice of an appropriate dose, the reduction in superior mesenteric blood flow was not accompanied by any changes in systemic arterial blood pressure, heart rate, and renal or hindquarters blood flows. Porcine neuromedin U-25 had similar effects to neuromedin U-8, but was generally more potent. In Brattleboro rats the pattern of response to neuromedin U-25 was similar to that seen in Long-Evans rats, indicating that mesenteric vasoconstriction was not dependent on release of endogenous vasopressin. In Long-Evans rats the regional hemodynamic actions of rat neuromedin U were comparable with those of porcine neuromedin U-25. The latter peptide at a dose of 1.0 nmol caused a rise in total peripheral resistance and a reduction in cardiac output, with an inconsistent change in heart rate. The results raise the possibility that the high concentration of neuromedin U in the rat intestine is associated with the control of local blood flow.
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PMID:Regional hemodynamic effects of neuromedin U in conscious rats. 230 45

Haemodynamic responses and antidiuretic hormone (ADH) were measured during body position changes designed to induce blood volume shifts in 10 cardiac transplant recipients to assess the contribution of cardiac and vascular volume receptors in the control of ADH secretion. Each subject underwent 15 min of a control period in the seated posture, then assumed a lying posture for 30 min at 6 degrees head-down tilt (HDT) followed by 30 min of seated recovery. Venous blood samples and cardiac dimensions (echocardiography) were taken at 0 and 15 min before HDT, 5, 15 and 30 min of HDT, and 5, 15 and 30 min of seated recovery. Blood samples were analysed for haematocrit, plasma osmolality, plasma renin activity (PRA) and ADH. Resting plasma volume (PV) was measured by Evans blue dye and per cent changes in PV during posture changes were calculated from changes in haematocrit. Heart rate (HR) and blood pressure (BP) were recorded every 2 min. In the cardiac transplant subjects, mean HR decreased (BP less than 0.05) from 102 b.p.m. pre-HDT to 94 b.p.m. during HDT and returned to 101 b.p.m. in seated recovery while BP was slightly elevated (P less than 0.05). PV was increased by 6.3% (P less than 0.05) by the end of 30 min of HDT but returned to pre-HDT levels following seated recovery. Plasma osmolality was not altered by posture changes. Mean left ventricular end-diastolic volume increased (P less than 0.05) from 90 +/- 5 ml pre-HDT to 105 +/- 4 ml during HDT and returned to 88 +/- 5 ml in seated recovery. Plasma ADH was reduced by 28% (P less than 0.05) by the end of HDT and returned to pre-HDT levels with seated recovery. PRA was also reduced by 28% (P less than 0.05) with HDT. These responses were similar to those of six normal cardiac-innervated control subjects and one heart-lung recipient. Therefore, cardiac volume receptors are not the only mechanism for the control of ADH release during acute blood volume shifts in man.
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PMID:Haemodynamic and ADH responses to central blood volume shifts in cardiac-denervated humans. 230 36

The role of endogenous vasopressin in cardiovascular homeostasis was examined using vasopressin-deficient rats (Brattleboro) (n = 194) and their parent strain, Long-Evans rats (n = 181). Mean arterial pressure (blood pressure) and heart rate were measured every 4 seconds with or without infusion of drug solution for 21 hours, and mean values and their standard deviations (lability) were calculated. Blood pressure in Brattleboro rats (116 +/- 1.1 mm Hg, mean +/- SEM) was significantly higher than that in Long-Evans rats (96 +/- 0.7 mm Hg, p less than 0.001), whereas heart rates (381 +/- 3.3 and 375 +/- 2.9 beats/min, respectively) were similar. The lability of blood pressure and heart rate in Brattleboro rats (9.2 +/- 0.1 mm Hg and 42.3 +/- 0.7 beats/min) was also greater than that in Long-Evans rats (6.7 +/- 0.1 mm Hg, p less than 0.001 and 38.4 +/- 0.8 beats/min, p less than 0.01, respectively). In Brattleboro rats, intravenous vasopressin (0.1 ng/kg/min or 0.6 ng/kg/min) did not affect blood pressure, although it did reduce heart rate and decreased lability of blood pressure and heart rate. Intracerebroventricular (central) infusion of vasopressin (2 pg/kg/min) in Brattleboro rats induced initial hypertension and tachycardia followed by long-lasting hypotension and bradycardia, whereas in Long-Evans rats it induced only hypertension and tachycardia. In both strains, central vasopressin dramatically decreased the lability of blood pressure and heart rate. Neither intravenous (0.2 ng/kg/min) nor central desmopressin (2 pg/kg/min or 0.2 ng/kg/min), a V2 renal receptor agonist, changed any of these parameters in Brattleboro rats, although both diminished urinary volume. Neither intravenous (50 ng/kg/min) nor central (3.3 pg/kg/min) d(CH2)5-Tyr(Me)-arginine vasopressin, a vasopressin V1 receptor antagonist, modulated any of these parameters in Long-Evans rats. These results suggest that endogenous as well as exogenous vasopressin acts centrally as a cardiovascular inhibitor and stabilizer through a receptor mechanism other than V1 or V2 receptor mechanisms.
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PMID:Cardiovascular depression and stabilization by central vasopressin in rats. 230 87

We applied [14C]deoxyglucose autoradiography and imaging techniques to determine rates of glucose metabolism in distinct subdivisions of the subfornical organ (SFO) of conscious Brattleboro rats. Seven anatomically-defineD SFO subregions were discerned having metabolic activities that differed from one another by as much as 29% in water-sated Brattleboro rats. The highest metabolic activity was found in the ventromedial zone of central and caudal subregions where previous studies identified the greatest densities of neurons, capillaries, putative angiotensin receptors, and angiotensin-immunoreactive fibers. Homozygous Brattleboro rats had rates of glucose metabolism that were 39-68% greater than those in corresponding SFO subregions of Long-Evans rats; these differences were accentuated by about 50% following 18 h of water deprivation. Exogenous treatment of Brattleboro rats with vasopressin uniformly normalized subregional glucose metabolism in the SFO. In Sprague-Dawley rats, water deprivation over 120 h provoked greater increases in metabolism of ventromedial than of dorsolateral SFO zones in amounts similar to the differences between Long-Evans and Brattleboro rats. The findings identify focal areas of high metabolic activity within subregions of the SFO where central responses are likely initiated to defend against homeostatic disturbances. The data represent further evidence for the probability that angiotensin II, as both hormone and neurotransmitter, is a metabolic stimulant of its target cells in the nervous system.
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PMID:Differential rates of glucose metabolism across subregions of the subfornical organ in Brattleboro rats. 230 47


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